Abstract

Toxoplasma gondii is a worldwide obligate intracellular protozoan parasite that infects humans and animals by either congenital or postnatal routes. Modulation of the immune system by infection with parasites is proposed to suppress the allergic inflammation. In this study we investigated whether experimental infection with T. gondii could induce the immune regulatory cells, including IL-10 producing CD1dhighCD5+ regulatory B cells (Bregs) and CD4+CD25+Foxp3+ regulatory T cells, and whether Breg induction was relevant to parasite immune escape during T. gondii infection. In vivo depletion studies demonstrated an important role for Bregs in T. gondii survival. Furthermore, adoptive transfer of Bregs isolated from T. gondii-infected mice enhanced cyst formation in brain of T. gondii-infected recipient mice. The present study was also investigated whether the development of allergic atopic dermatitis (AD) could be suppressed by T. gondii infection in murine. T. gondii infection substantially suppresses the development AD-like lesions induced by allergen Dermatophagoides farinae in NC/Nga mice, a model of human AD. Collectively, these results indicate that induction of Breg and Treg during T. gondii infection are necessary for evasion of host immunity, and, as the bystander suppressive effect, these cells could suppress allergic inflammation.